Severity
Systolic pressure gradient [mmHg]
Area of valve opening [cm2]
I
<40
>1.5
II
40–80
0.8–1.5
III
81–120
0.4–0.8
IV
>120
<0.4
Aortic valve stenosis increases systolic resistance. The increased left ventricle pressure strain causes concentric left ventricle hypertrophy. The pressure volume curve is pushed up and to the right. With increasing hypertrophy, a compliance disorder develops so that over the clinical course, the left ventricular end-diastolic pressure and, secondly, the pressure in the left atrium increase (see Fig. 9.1).
Fig. 9.1
Pressure–volume curve of the left ventricle. In aortic valve stenosis, the thickened myocardium of the left ventricle is less flexible (reduced compliance). Therefore, the pressure volume curve moves up and to the right (dotted line). There is increased end-diastolic pressure and volume (a → a′). Since the left ventricle must pump against a fixed gradient (increased afterload), the endpoint of the isovolumetric contraction also shifts (b → b′)
The increased basal myocardial energy and oxygen demand are a result of the pressure burden by the increased cardiac myocardial mass [4]. Coronary perfusion may not be sufficient for the increased demand so that myocardial ischemia may arise. Reasons for decreased myocardial perfusion are:
Inadequate vascularization of the myocardium for the proportionately large muscle mass
A reduced coronary perfusion gradient due to increased end-diastolic pressure and decreased post-stenosis pressure in the aorta and due to an increased diffusion pathway through the hypertrophied myocardium
If myocardial ischemia occurs, the left ventricle may react with serious arrhythmias, including ventricular fibrillation. The clinical symptoms, which tend to appear during physical exertion, are:
Angina pectoris without evidence of coronary artery stenosis
Fainting (cardiac syncope)
Acute heart failure
>> After all these thoughts went through Dr. Casey’s head, he discussed general anesthesia with Mrs. Taylor. She became a little upset, because her previous surgeries had gone well with spinal anesthesia. Dr. Casey explained why a spinal was now contraindicated, and he promised to prescribe a sedative for her to take before bed.
Mrs. Taylor actually slept well. The surgery was planned for the morning, so she didn’t eat breakfast. However, as she was about to leave for the hospital, a nurse phoned her to tell her that her surgery would be delayed until 1 p.m., due to an emergency.
Dr. Diana was assigned to do the anesthesia, a resident with 2 years of anesthesia experience. Reviewing the medical record and preoperative evaluation, she stumbled upon the patient’s comorbidities. Dr. Diana wondered if she should call the attending anesthesiologist, Dr. Eldridge, to discuss the case; but then she decided not to. She was sure that he had been informed about Mrs. Taylor yesterday. In addition, he was supposed to see the patient himself in the preoperative area. Dr. Eldridge told Dr. Diana to get started with the patient’s anesthesia and he would be in shortly. “We’ll use the ProSeal laryngeal mask airway,” she said to the anesthesia technician Freya. Due to Mrs. Taylor’s unremarkable previous anesthetics and the expected short duration of the surgery, Dr. Diana saw no reason to deviate from routine anesthesiology techniques, which she had mastered.
Mrs. Taylor was positioned in the lithotomy position; a 5–lead ECG, blood pressure cuff, oxygen saturation clip, and an IV infusion were all set up. The blood pressure was 150/80 mmHg; the heart rate was 55 beats/min. After preoxygenation, she received 150 μg fentanyl and 150 mg propofol IV.
Dr. Diana placed the ProSeal laryngeal mask airway, size 4, without incident and mechanically ventilated the patient with pressure–controlled ventilation due to the patient’s obesity. In order to maintain anesthesia, Dr. Diana turned on the desflurane vaporizer. “Doing well,” she thought and informed the experienced gynecological team that they could begin.
The next blood pressure reading, the first after induction, showed pronounced hypotension, at 70/50 mmHg, with a pulse of 65 beats/min (which was a slight increase from the preinduction pulse). Dr. Diana increased the IV fluids and gave phenylephrine 200 μg IV. Dr. Diana briefly considered giving more fluids, but then she remembered that because of the left ventricular pressure load, the left atrium was probably strained, and a relative mitral valve regurgitation could occur, leading to pulmonary edema. So, she decided against it.
The next blood pressure was 80/60 mmHg, and Mrs. Taylor received additional phenylephrine 250 μg. “She’s responding, but slowly,” thought Dr. Diana. The gynecologists picked up on her increasing nervousness. “Is something wrong?” asked one of them. “No, no.” Dr. Diana replied and then asked, “Is it bleeding a lot?” The gynecologist responded, “No more than usual. In 3 min we’ll be finished.”
Dr. Diana relaxed upon hearing the news and shut off the desflurane vaporizer. Suddenly Mrs. Taylor’s heart rate fell to 30 beats/min. Dr. Diana hit the off button for the monitor’s alarm and opened the medication drawer of the anesthesia cart as fast as she could to get some atropine. She yelled for Freya to help out. The anesthesia technician was in another OR helping during induction of anesthesia. When Freya did enter the OR, she saw Dr. Diana with a vial of atropine and the monitor: the ECG showed a flat line. There was no alarm – asystole.
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